Escherichia coli B is uIiusually sensitive to ultraviolet light (UV), compared to other wild-type strains and to its own radiation-resistant derivatives such as B/r. 1 Despite the large difference in survival after exposure to the same dose of UV, strains B and B/r differ little, or not at all, in:(1) number of thymine-containing dimers produced in the DNA, 2 (2) rate at which thymine-containing dimers are excised from the DNA, 2 (3) ability to promote" host-cell reactivation" of irradiated bacteriophages, 3 and (4) recovery time and rate of synthesis of DNA after irradiation. 4 Sensitivity to UV in strain B, unlike that in certain other UV-sensitive strains isolated from both B and B/r, is not associated with reduced ability to re-pair pyrimidine dimersor other kinds of UV damage that block DNA replication. The most striking difference between strains B and B/r is the failure of cell division in the sensitive strain after exposure to very low doses of UV, resulting in the formation of greatly elongated filamentous cells upon subsequent incubation.'Survivors and nonsurvivors alike form filaments, the survivors ultimately regaining the ability to divide. Agents other than UV (eg, crystal violet5 and nitroso-guanidine6) also cause filamentous growth in B but not in B/r, and similar" snakes" are frequently observed in untreated cultures of the sensitive strain. Strains B and B/r differ mainly in the vulnerability of the cell division mechanism, which in strain B is readily deranged by a variety of initiating stimuli. In B/r given the same treatments, inhibition of the cell division mechanism either is not initiated or is promptly and invariably reversed.

Impressive similarities have been noted7'8 between filament formation in strain B and prophage induction in lysogenic strains such as K12 (X), some of which are summarized below:(1) Both filament formation and prophage induction are mass effects, occurring in virtually every member of a population exposed to low doses of UV.(2) Both effects can be initiated by a variety of agents other than UV, all having in common the ability to produce damaging changes in DNA. Although no systematic comparison has been made to determine whether the same agents invariably produce both effects, strainB is more sensitive than strain B/r to many of the agents known to cause prophage induction (X rays,'mitomycin C, 9 and nitrogen mustard'0).(3) Both filament formation inB and prophage induction in K12 (X) occur occasionally in untreated cultures, and especially in" old" cultures. 6 (4) UV-initiated filament formation is photoreversible," 1 as is prophage induction; 12 that is, both are greatly reduced by post-UV exposure to visible light. In strain B, efficient photoreactivation is obtained when wavelengths of light responsible for indirect effects are excluded, and most of this photoreactivation can be ascribed to the enzymatic splitting of pyrimidine dimers. 13 The same appears to be true of prophage induction in K12 (X). 6 This indicates that both effects when produced by UV depend upon the presence in the DNA of pyrimidine dimers. The doses of